Human sleep/waking patterns undergo significant changes with advancing age. Decreased stage 4 and REM sleep and increased nighttime wakefulness are consistent findings in sleep studies of the aged. We hypothesize that this age-related disruption in sleep patterns, observed even in very healthy non-complaining aged individuals, may be related to an age-change in sympathetic nervous system (SNS) activity. There is considerable anatomical, physiological and pharmacological evidence that indicates the central mechanisms regulating sleep/waking patterns and SNS outflow may interact. Plasma norepinephrine (NE) levels, which increase with age, are thought to be markers of SNS activity; plasma NE is increased following SNS activation by a variety of stimuli and decreased by pharmacological inhibition. Individual levels of nighttime plasma NE correlate with degree of disturbed sleep among aged individuals, while experimentally induced alterations of sleep patterns do not affect plasma NE levels. Finally, increasing SNS activity via hypovolemia induced by low sodium diet results in both increased plasma NE and disruption of sleep patterns in preliminary studies of young adults. The proposed study will examine the effects of low, normal and high levels of dietary sodium on the sleep and nighttime physiology of young and aged normal men. This will test our hypothesis that central SNS activity level affects sleep. We predict that increased SNS activity induced by hypovolemia (resulting from low sodium diet) will be associated with higher plasma NE and disturbed sleep. Conversely, inhibiting SNS activity by high sodium diet should decrease plasma NE and either improve, or have no effect on sleep patterns. If altering SNS activity is found to affect sleep patterns, this would suggest new approaches to the treatment of sleep complaints in some aged populations.